Capita Foundation is a nonprofit organization that funds hearing research scientists with micro-grants to innovate. Our seed grants encourage researchers to think outside the box and explore fearlessly in prevention and cure of hearing disorders.
Over the past decade of micro-grants our Capita awardees have averaged a 10 fold return with subsequent [NIH, NSF, etc] funding.

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Project Title: “Investigating the Temporal Resolution Capacity in School Aged Children via Neurophysiological Measurement. Pilot Study.”Prof. Koravand's research deals with the relationship between the peripheral and central auditory systems in children. Her goal is to develop neurophysiological measures (biological markers) to assess the central auditory functions of children during early childhood, to prevent disorders while brain plasticity is still significant.

Daniel A. Llano, M.D., Ph.D.

In our research program, we will examine the impact of aging on the auditory system. We will focus on developing innovative approaches to measure metabolic changes in the aging auditory system and developing novel interventions to mitigate them. Successful completion of this work will lead to new approaches to preserve hearing as we age.

Josée Lagacé, Ph.D. and Benoît Jutras , Ph.D.

University of OttawaProject Title: "Virtual Reality For Auditory Training Therapy: A Pilot Study"

Virtual reality (VR) allows an individual to interact in real time with a three-dimensional, computer-simulated environment. The objective of this pilot study is to evaluate VR as an effective interface for ensuring uptake and motivation to auditory training in children with auditory processing difficulties. Since many children with auditory processing difficulties also have learning problems at school, this approach could also contribute to the enhancement of their learning experience and as well as to a reduction of schooling failure.

Madhu Sundarrajan, Ph.D.

University of the PacificProject Title: “Audiological and Communication Outcomes in Children with Unilateral Hearing Loss: A Pilot Study.”

Unilateral hearing loss (UHL) or single-sided deafness is a type of hearing impairment where individuals have typical hearing in one ear and impaired hearing in the other ear. Permanent UHL exists when the average pure tone air conduction threshold at 0.5, 1, and 2 kHz is greater than or equal to 20 dB HL or pure tone air conduction thresholds are greater than 25 dB HL at two or more frequencies above 2 kHz in the affected ear with an average pure tone air conduction threshold in the good ear less than or equal to 15 dB (National Workshop on Mild and Unilateral Hearing Loss 2005). It is estimated that 1/3 of children with hearing loss are diagnosewith UHL (Lieu, 2018).

Historically UHL was typically not treated in children with the presumption that the contra-lateral ear with hearing levels within the typical range will suffice in providing adequate acoustic stimuli for development of speech perception and communication skills (Oyler, Oyler & Matkin, 1987). However, recent research has shown that children with untreated UHL have poorer communication and academic outcomes compared to typical hearing (TH) children (Kishon-Rabin, Kuint, Hildesheimer, & Ari-Even, 2015, Fitzpatrick et al., 2018; Lieu, 2018), indicating that children with UHL may benefit from an amplification device fitted to the poorer ear.

This project aims to ameliorate the critical gap in the literature by comprehensively investigating audiological and communication outcomes in children with UHL. Furthermore, this project will provide vital information regarding clinical recommendations for children with UHL, in order for them to maintain age appropriate auditory, communication and academic outcomes.Matthew J. Wilson, Ph.D.Northern Illinois University

Project Title: “Relationship Between Cognitive Changes and Speech-in-Noise Deficits in Individuals with a History of Concussion: An Efferent System Study.”

It is well known that long-standing cognitive deficits in the areas of attention and memory frequently accompany concussion. The role that these cognitive deficits play in the development of auditory processing difficulties, such as trouble understanding speech in noise (SIN), following injury remains unclear. Processing auditory information requires a complex interaction between afferent and efferent auditory pathways. The nature of the relationship is such that afferent information, which travels from cochlea to cortex, can be modulated by top-down, cortical influences via feedback loops in the efferent system (ES). These loops are integral for a variety of auditory skills, like understanding SIN. ES strength can be non-invasively measured using a technique known as otoacoustic emission (OAE) suppression, which quantifies how well outer hair cell activity is suppressed in the presence of noise. Greater levels of suppression are indicative of stronger ES activation and have been shown to correlate with better auditory comprehension abilities.

The interdependence of the cortex and efferent pathway suggests that alterations in cortical activity, like what is seen following concussion, may have an impact on overall suppression levels and, by default, play a role in the development of SIN difficulties; however, the nature of the relationship remains poorly understood. Thus, this study aims to examine the relationship between electrophysiological indices of cognition and SIN abilities and how those relate to changes in behavioral performance. Finding will not only improve audiological diagnosis, treatment, and rehabilitation options, but will also expand the role of the audiologist in the area of head injury research.

During all of our life, we are surrounded by sounds that include different frequencies and intensity levels. In the inner ear, the sensory hair cells pick up the sound signal and transmit it to auditory nerve fibers via chemical synapses by releasing the transmitter glutamate; and auditory nerve fibers transmit the sound-coding signal to the brain.Sound intensity is encoded by the amount of glutamate released by the hair cell, leading to glutamate receptor activation and then action potential firing in auditory nerve fibers. During noise exposure, it has been described that auditory nerve fiber endings can be damaged short- or long-term, most likely due to and excess of calcium influx into the auditory nerve fiber endings. This phenomenon is called excitotoxicity, however, the underlying mechanisms are not completely understood.

Here I propose to investigate molecular mechanisms of synaptic transmission between hair cells and auditory nerve fibers and to test how they are affected after noise trauma.

Valerio Magnaghi, Ph.D.

Vestibular Schwannoma is a benign tumor of the acoustic nerve causing hearing loss. It arises from Schwann cells, the main myelin-forming cells in the nerve. Thus, changes in the oncogenic properties of these cells may be involved in hearing loss.

The main goal of our project is to analyze the molecular mechanisms underlying the human Schwann cells oncogenic transformation, potentially responsible of the vestibular schwannoma onset, and their vulnerability to environmental electromagnetic fields, that in principle might be pathologically relevant for the hearing loss.

Alisha L. Jones, Au.D., Ph.D., CCC-A

Acceptable noise levels have been found to assist in predicting potential success with hearing aids. If we can find a way to lower a person’s acceptable noise level, then their potential for success with hearing aids might increase. This project will examine the effects of three different computer-based aural rehabilitation programs on acceptable nose levels in adults with hearing loss.

The overall goal of my project is to study the effect of sex hormones on hearing loss due to noise in female mice.

Noise induced hearing loss is a permanent hearing impairment common in our society resulting from prolonged exposure to high levels of noise. Recent findings demonstrated that the circadian rhythms plays an important role in modulating auditory sensitivity to noise trauma. Mice day-exposed to noise recovered to normal hearing thresholds compared to the nigh-exposed ones. This diurnal variation demonstrates the result of strict interaction between hormones like glucocorticoids and the circadian cochlear clock. Sex hormones like estrogen have also a circadian regulation but most of the published studies on noise-induced hearing loss (NIHL) used male only even if NIHL affects both men and women. Therefore, a new study is needed to better explain the effect of sex hormones on hearing loss due to noise in females to better understand the potential role of estrogen receptor signaling in the auditory system.

Victor Wong, Ph.D.

My long-standing research interests lie in identifying molecular mechanisms for axonal regeneration after nervous system disease or injury. Axons in the adult central and peripheral nervous systems have little capacity to regenerate after injury. Although hearing regenerative capacity have been documented in avian and amphibian species, the reversal of hearing loss in mammals has been a persistent challenge. Most therapeutic strategies have focused on the replacement of hair cells (HCs); however, HC replacement has been largely ineffective since subsequent degeneration of the innervating spiral ganglion neuron (SGN) peripheral neurites severely compromises efforts for functional recovery of hearing. Both the success of cochlear implants (CI) and of future therapeutic approaches critically depend on the integrity of SGNs and the availability of functional neurites for direct stimulation. Moreover, very little is known about how to promote SGN neurite growth. There is, therefore, a critical and unmet need to determine how to enhance SGN peripheral neurite growth. The neuronal processes contain a network of cytoskeletal structures necessary to steer neurite outgrowth and maintain structural integrity. Such structures comprise of actin and microtubules that are under the influence of extrinsic cues, thereby affecting their stability, dynamics, and the ability to re-direct neurite growth. Moreover, changes in actin and microtubule dynamics have been implicated to impact transport of important cargoes such as mitochondria and mRNAs in the neuronal processes. These biological processes are necessary to re-establish proper innervation and circuit assembly. Therefore, the main objective of my research is to understand 1) how changes in microtubule dynamics affect neurite growth under pathological conditions, 2) how axonal transport is regulated by microtubule stability, and 3) how to capitalize these biological processes (i.e., microtubule dynamics and axonal transport) into therapeutic strategies to encourage neural regeneration and repair.

Dunia Abdul-Aziz, M.D.

Loss of inner ear hair cells is the predominant cause of hearing loss. High throughput screening of drug libraries for compounds that may promote hair cell regeneration has until now been precluded by the relatively few number of cells that can be derived from the mammalian cochlea. Our lab has recently established a protocol for expansion of inner ear progenitor cells in culture, thereby generating “inner ear organoids” which can be used to study pathways in inner ear development.

We propose to design an Atoh1-reporter system in which the regulatory elements of the key hair cell- fate determining gene, Atoh1, drive luciferase signal. Delivery of this reporter into inner ear organoids allows us to directly study, in a high throughput fashion, the regulation of Atoh1 in primary hair cell progenitors. We propose to use this organoid-based reporter system to test the effects of candidate genetic /epigeneticmodifying drugs on Atoh1 activity. This will serve as one of potentially several applications of this reporter system in drug and genetic screening.

Dr. Andrew Wise

Bionics Institute, Melbourne, Australia

Project: Drug delivery to the cochlear for synaptic repairThe Problem: Most adult people, including you and I, are likely to have damaged the highly sensitive sensory cells in our inner ear (see image). We will be disappointed to learn from our doctor that there are no therapeutic options to treat this damage and that unfortunately our condition is likely to worsen over time. There is desperate need to develop drug therapies that can treat, or possibly reverse hearing loss.Project Aims: We have developed a novel way to deliver medication to the inner ear using specially designed particles that are made using nanoengineering techniques. In order to develop this system for use in the clinic we need to test their effectiveness in delivering medication into the inner ear. Therefore, the aim of this project is to measure the levels of medication inside the inner ear following delivery using the particle system. Outcomes of this study will be critical in further developing the technology so that it can be used to treat hearing loss in the clinic.

A primary cause of hearing loss is damage to the sensory cells in the inner ear – the hair cells and neurons that are responsible for detecting and transmitting sound information to the brain. What we are beginning to understand is that the sensitive connections (red dots – arrow) between the sensory hair cells (blue cell) and the neurons (green cells) are highly susceptible to damage. We are developing drug therapies to ‘reconnect’ the cochlea to treat hearing impairment.

**PLOS ONE publication by Valeriy Shafiro, Ph.D.

Capita Foundation is pleased to announce that Valeriy Shafiro, Ph.D., who was awarded a grant from us in 2012 for a research project titled, "Environmental sound and speech perception in relation to language development in children with cochlear implants," has recently published a research report in PLOS ONE.

Amanda Lauer, Ph.D.

Johns Hopkins University, Dept. of Otolaryngology

Project Title: “Optimizing hearing with top-down brain control of the ear.”

Project Description

The overall goal of my research is to understand how auditory input from the ear affects the brain, and how the brain in turn affects the ear through efferent feedback loops. I am particularly interested in understanding the hearing disorders that develop when input to and from the brain is altered. We propose to study top-down efferent effects on hearing to understand how the brain controls the ear using optogenetic, behavioral, and immunohistochemical techniques in rodent models. Understanding how these pathways work may open up new treatment avenues for hearing disorders and will help us understand how hearing is optimized by top-down brain control of cochlear activity.

Medial (MOC) and lateral olivocochlear (LOC) neurons project from the brain to the ear and control information sent back to the brain. Adapted from Lauer et al. (2012). Neurobiology of Aging.

Sanjee Abeytunge

The ear is the fastest and most sensitive sensory organ in the human body. It can resolve data a thousand times faster than the eye and can detect vibrations in the environment at the atomic-scale. The dynamic range of human hearing embraces up to 120 dB of sound-pressure level (SPL). This dynamic range allows humans to hear a millionfold range of amplitudes. The frequency response of a human ear extends to 20 kHz while other mammals, such as whales and bats, can hear up to hundreds of kilohertz. However, the current stimulation probes of hair cells in the cochlea, the sense organ of the ear, to study the mechanics of the inner ear is limited to less than 1 kHz. This limitation leaves most of the mammalian auditory frequencies unstudied. This experimental limitation is due to the physical dimensions of the probes and their configurations used during experiments. My work is design and construction of a micrometer scale novel probe that will overcome the current frequency limitation.